Signature of frustrated moments in quantum critical CePd1−x_{1-x}Nix_xAl

CePdAl with Ce $4f$ moments forming a distorted kagom\'e network is one of the scarce materials exhibiting Kondo physics and magnetic frustration simultaneously. As a result, antiferromagnetic (AF) order setting in at $T_{\mathrm{N}} = 2.7$~K encompasses only two thirds of the Ce moments. We report measurements of the specific heat, $C$, and the magnetic Gr\"uneisen parameter, $\Gamma_{\rm mag}$, on single crystals of CePd$_{1-x}$Ni$_x$Al with $x\leq 0.16$ at temperatures down to 0.05~K and magnetic fields $B$ up to $8$~T. Field-induced quantum criticality for various concentrations is observed with the critical field decreasing to zero at $x_c\approx 0.15$. Remarkably, two-dimensional (2D) AF quantum criticality of Hertz-Millis-Moriya type arises for $x=0.05$ and $x=0.1$ at the suppression of 3D magnetic order. Furthermore, $\Gamma_{\rm mag}(B)$ shows an additional contribution near $2.5$~T for all concentrations which is ascribed to correlations of the frustrated one third of Ce moments.Comment: 5+2 pages with 4+3 figure

Strong Valence Fluctuation Effects in SmTr2Tr_2Al20_{20}(Tr=Tr=Ti, V, Cr)

We present a single crystal study of low temperature magnetism and transport in Sm$Tr_2$Al$_{20}$ ($Tr =$ Ti, V and Cr). Strong valence fluctuation is manifested as Kondo effects including a large Sommerfeld coefficient $\gamma$, a weak temperature dependence of magnetic susceptibility and a $-\ln T$ dependent resistivity. All the systems order antiferromagnetically at $T_{\rm N}=$ 6.4 K (Ti), 2.3 K (V) and 1.8 K (Cr). Systematic change in the susceptibility, specific heat, and resistivity indicates that stronger $c$-$f$ hybridization in SmV$_2$Al$_{20}$ and SmCr$_2$Al$_{20}$ than in SmTi$_2$Al$_{20}$ suppresses $T_{\rm N}$ and induces the valence fluctuations and moreover field insensitive heavy fermion states

慢性肝炎患者における血清中および異なる3ケ所の肝組織中C型肝炎ウイルスのQuasispecies(擬均一性)の検討

取得学位：博士(医学), 学位授与番号：医博乙第1501号，学位授与年月日：平成11年10月6日,学位授与年：199

非磁性G3基底2重項を持つ立方晶PrTr2Al(20) (Tr = Ti, V)における混成効果と超伝導

学位の種別:課程博士University of Tokyo(東京大学

Peretinoin, an acyclic retinoid, improves the hepatic gene signature of chronic hepatitis C following curative therapy of hepatocellular carcinoma

BACKGROUND: The acyclic retinoid, peretinoin, has been shown to be effective for suppressing hepatocellular carcinoma (HCC) recurrence after definitive treatment in a small-scale randomized clinical trial. However, little has been documented about the mechanism by which peretinoin exerts its inhibitory effects against recurrent HCC in humans in vivo. METHODS: Twelve hepatitis C virus-positive patients whose HCC had been eradicated through curative resection or ablation underwent liver biopsy at baseline and week 8 of treatment with either a daily dose of 300 or 600 mg peretinoin. RNA isolated from biopsy samples was subjected to gene expression profile analysis. RESULTS: Peretinoin treatment elevated the expression levels of IGFBP6, RBP1, PRB4, CEBPA, G0S2, TGM2, GPRC5A, CYP26B1, and many other retinoid target genes. Elevated expression was also observed for interferon-, Wnt-, and tumor suppressor-related genes. By contrast, decreased expression levels were found for mTOR- and tumor progression-related genes. Interestingly, gene expression profiles for week 8 of peretinoin treatment could be classified into two groups of recurrence and non-recurrence with a prediction accuracy rate of 79.6% (P<0.05). In the liver of patients with non-recurrence, expression of PDGFC and other angiogenesis genes, cancer stem cell marker genes, and genes related to tumor progression was down-regulated, while expression of genes related to hepatocyte differentiation, tumor suppression genes, and other genes related to apoptosis induction was up-regulated. CONCLUSIONS: Gene expression profiling at week 8 of peretinoin treatment could successfully predict HCC recurrence within 2 years. This study is the first to show the effect of peretinoin in suppressing HCC recurrence in vivo based on gene expression profiles and provides a molecular basis for understanding the efficacy of peretinoin